ArticleJournal of the American Society of Nephrology : JASN2012
MicroRNA-324-3p promotes renal fibrosis and is a target of ACE inhibition.
Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 95 citations in OpenAlex.
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- Urinary miR-221-3p and miR-324-5p in combination with albuminuria as a promising model for non-invasive diagnosis of pediatric celiac disease.Scientific reports · 2026Article
- Pathogenesis of Focal Segmental Glomerulosclerosis and Related Disorders.Annual review of pathology · 2025Review
- Epigenetics of Hypertensive Nephropathy.Biomedicines · 2024Review
- Epigenetic DNA Methylation and Protein Homocysteinylation: Key Players in Hypertensive Renovascular Damage.International journal of molecular sciences · 2024Review
- Gallic Acid Alleviates Glucolipotoxicity-Induced Nephropathy by miR-709-NFE2L2 Pathway in db/db Mice on a High-Fat Diet.Journal of agricultural and food chemistry · 2024Article
- Identification and Validation of the miR/RAS/RUNX2 Autophagy Regulatory Network in AngII-Induced Hypertensive Nephropathy in MPC5 Cells Treated with Hydrogen Sulfide Donors.Antioxidants (Basel, Switzerland) · 2024Article
- Abnormal Expression of Prolyl Oligopeptidase (POP) and Its Catalytic Products Ac-SDKP Contributes to the Ovarian Fibrosis Change in Polycystic Ovary Syndrome (PCOS) Mice.Biomedicines · 2023Article
- Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023Review
- Association between angiotensin-converting enzyme inhibitor-induced cough and the risk of lung cancer: a Mendelian randomization study.Frontiers in pharmacology · 2023Article
- A review on the role of miRNA-324 in various diseases.Frontiers in genetics · 2022Review
- Molecular profiling of urinary extracellular vesicles in chronic kidney disease and renal fibrosis.Frontiers in pharmacology · 2022Review
- Integrative genomic analysis of blood pressure and related phenotypes in rats.Disease models & mechanisms · 2021Article
- Long Non-coding RNA ENST00000453774.1 Confers an Inhibitory Effect on Renal Fibrosis by Inhibiting miR-324-3p to Promote NRG1 Expression.Frontiers in cell and developmental biology · 2021Article
- Metabolic reprogramming by N-acetyl-seryl-aspartyl-lysyl-proline protects against diabetic kidney disease.British journal of pharmacology · 2020Article
- Targeting the progression of chronic kidney disease.Nature reviews. Nephrology · 2020Review
- miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive mice.European journal of medical research · 2020Article
- Article
- Emerging role of miRNAs in renal fibrosis.RNA biology · 2020Review
- Diabetic Nephropathy: Novel Molecular Mechanisms and Therapeutic Targets.Frontiers in pharmacology · 2020Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contribution of microRNA (miRNA) to the pathogenesis of renal fibrosis is not well understood. Here, we investigated whether miRNA modulates the fibrotic process in Munich Wistar Fromter (MWF) rats, which develop spontaneous progressive nephropathy. We analyzed the expression profile of miRNA in microdissected glomeruli and found that miR-324-3p was the most upregulated. In situ hybridization localized miR-324-3p to glomerular podocytes, parietal cells of Bowman's capsule, and most abundantly, cortical tubules. A predicted target of miR-324-3p is prolyl endopeptidase (Prep), a serine peptidase involved in the metabolism of angiotensins and the synthesis of the antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP). In cultured tubular cells, transient transfection with a miR-324-3p mimic reduced Prep protein and activity, validating Prep as a target of this miRNA. In MWF rats, upregulation of miR-324-3p associated with markedly reduced expression of Prep in both glomeruli and tubules, low urine Ac-SDKP, and increased deposition of collagen. ACE inhibition downregulated glomerular and tubular miR-324-3p, promoted renal Prep expression, increased plasma and urine Ac-SDKP, and attenuated renal fibrosis. In summary, these results suggest that dysregulation of the miR-324-3p/Prep pathway contributes to the development of fibrosis in progressive nephropathy. The renoprotective effects of ACE inhibitors may result, in part, from modulation of this pathway, suggesting that it may hold other potential therapeutic targets.
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